{"id":"bd46fe688be5","type":"article","url":"https://hartvaat.nl/2026/10/01/masld-verhoogt-sterfte-en-cv-risico-onafhankelijk-van-lipoproteine-a/","title":"MASLD verhoogt sterfte- en CV-risico, onafhankelijk van lipoproteïne(a)","title_en":"The association of MASLD, lipoprotein(a) and long-term outcomes: Results from the multi-ethnic study of atherosclerosis.","category":"cholesterol","category_label":"Cholesterol","professions":["cardioloog","huisarts","internist"],"tags":[],"journal":"Metabolism: clinical and experimental","doi":"10.1016/j.metabol.2026.156723","source_url":"https://doi.org/10.1016/j.metabol.2026.156723","authors":["Gomathy Nageswaran","Vignesh Chidambaram","Amudha Kumar","Rami Doukky","Thorsten Leucker","Subhi J Al'Aref","Ragesh Thandassery"],"significance":5,"published":"2026-08-27","source_date":"2026-10-01","image":"","kennis":["https://hartvaat.nl/kennis/lipiden/lpa-meten-wanneer-waarom/","https://hartvaat.nl/kennis/lipiden/lp-a-verhoogd/"],"congress":"","summary_en":"A secondary analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) demonstrates that metabolic dysfunction-associated steatotic liver disease (MASLD) is linked to lower lipoprotein(a) [Lp(a)] levels but independently increases long-term mortality and cardiovascular risk. Patients with MASLD and elevated Lp(a) faced a twofold higher risk of hard cardiovascular events (HR 2.07), while those with MASLD and low Lp(a) still had a 28% higher all-cause mortality risk (HR 1.28). These findings highlight MASLD as an independent predictor of poor long-term outcomes, suggesting that Lp(a) measurement may refine risk stratification in patients with fatty liver disease.","created":"2026-08-21T00:47:53Z","updated":"2026-08-21T00:47:53Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Een secundaire analyse van de MESA-cohortstudie toont aan dat metabale dysfunctie-geassocieerde steatose van de lever (MASLD) samenhangt met lagere lipoproteïne(a)-spiegels, maar wel onafhankelijk van deze waarden het risico op all-cause mortaliteit en harde cardiovasculaire gebeurtenissen verhoogt. Patiënten met MASLD en verhoogde Lp(a) hadden een tweemaal hoger CV-risico (HR 2,07), terwijl MASLD met lage Lp(a) het sterfterisico met 28% verhoogde (HR 1,28). Deze bevindingen onderstrepen dat MASLD een zelfstandige risicofactor is voor langdurige mortaliteit en dat Lp(a)-meting extra risicoinformatie kan bieden bij levervetziekte.","abstract_original":"BACKGROUND AND AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with an increased risk of cardiovascular events and frequently coexists with other atherosclerosis risk factors, including obesity, metabolic syndrome, sleep apnea, and insulin resistance. Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like particle bound to apolipoprotein(a), that has been studied to have pro-thrombotic and pro-inflammatory properties and is an established independent risk factor for atherosclerotic disease. However, the association between MASLD and Lp(a) and their impact on long-term clinical outcomes have not been evaluated previously. METHODS: We performed a secondary analysis of the prospectively collected data from the Multi-Ethnic Study of Atherosclerosis (MESA). Baseline MASLD was defined as either a liver-to-spleen (L:S) attenuation ratio less than 1.0 or liver attenuation <40 HU on computed tomography (CT) imaging, excluding individuals with excess alcohol consumption (>15 drinks/week for men and > 10 drinks/week for women) and the presence of at least one cardiometabolic risk factor, including elevated BMI or waist circumference, type 2 diabetes mellitus, hypertension, hypertriglyceridemia, or reduced HDLC. Baseline Lp(a) levels were measured using a latex-enhanced turbidimetric immunoassay (Denka Seiken, Tokyo, Japan). RESULTS: Median Lp(a) levels were significantly lower in those with baseline MASLD compared to those without MASLD (11.9 vs 18.1 mg/dL, p-value <0.001). Individuals with MASLD and low Lp(a) levels (≤ 50 mg/dL) had a significantly higher risk of all-cause mortality compared to those without MASLD and with low Lp(a) (HR 1.28; 95% CI: 1.025-1.56), independent of traditional cardiovascular risk factors. Additionally, individuals with baseline MASLD and elevated Lp(a) were independently associated with an increased risk of hard cardiovascular disease (HR 2.07, 95% CI: 1.39-3.09), compared to individuals without MASLD and with Lp(a) ≤ 50 mg/dL. CONCLUSIONS: MASLD is independently associated with lower levels of Lp(a). Patients with baseline MASLD and elevated levels of Lp(a) exhibit nearly twice the risk of cardiovascular diseases as compared to the cohort with no MASLD and lower Lp(a) levels. Importantly, even in the absence of elevated Lp(a), MASLD is associated with increased all-cause mortality. These findings suggest that while Lp(a) is a strong contributor to cardiovascular risk, MASLD itself is an independent determinant of long-term mortality."}